Fig 2: Expression of FGFR2 in tissues from patients with NPC and in NPC SUNE1, C666-1, 6-10B and HNE-3 cell lines. (A) Microscopy images demonstrating FGFR2 expression in cancer and normal adjacent tissues, indicating the different levels of positive staining by immunohistochemistry. (B) Relative mRNA and (C) protein expression levels of FGFR2 in SUNE1, C666-1, 6-10B and HNE-3 cell lines. (D) Survival curves of NPC patients with low or high FGFR2 expression. Data are presented as mean ± standard deviation. ##P<0.01 vs. NP69 cell line. NPC, nasopharyngeal carcinoma; FGFR2, fibroblast growth factor receptor 2.

Fig 3: Levels of Fgfrs are altered in the lenses of Dlg10CRE mice.(A) RIPA, triton soluble (cytosolic) and triton insoluble (cytoskeletal-associated) extracts from P2 control and Dlg10CRE lenses were subjected to western blot analysis for Fgfr1, Fgfr2, and Fgfr3 and the blots reprobed for Gapdh as a loading control. Representative blots are shown. (B) Quantification of protein levels. Shown are the levels of each Fgfr in extracts from Dlg10CRE lenses relative to levels in the control (control levels set at 1.0). Signal intensities were quantified by phosphorimager analysis, as described in Materials and Methods, and the data subjected to statistical analysis using the two-sided One Sample t-test. At least 3 protein pools were analyzed in triplicate over 1–3 blots. The relative levels of Fgfr2 were reduced in the whole cell extract and cytoskeletal associated fraction compared to controls whereas the levels of Fgfr1 were increased as compared to controls. Error bars = standard deviations. * = FDR<0.05, ** = FDR<0.01.

Fig 4: Expression of FGFR1-4 in intact and injured mouse sciatic nerve. (A) RT-PCR showing FGFR1-4 mRNA expression in control and 7 days post-injury mouse sciatic nerve. (B) Data showing expression of FGFR1–3 mRNA at 7 days post-injury from mRNA sequencing data set GSE103039. (C) Fold difference of FGFR1 and FGFR2 against FGFR3 analyzed with the mRNA sequencing data set GSE103039. (D) The expression value of FGFR1–3 in cultured Schwann cells in our microarray data set GSE123915. (E) Western blot results showing that FGF5 inhibits the basal levels of ERK1/2 activity in cultured rat primary Schwann cells. (F) Western blot results showing that FGF5 significantly upregulates N-cadherin expression in Schwann cells after 4, 6, 8, and 10 h treatment. (G) Quantification of three independent western blot results for ERK1/2 inhibition by FGF5. (H) Quantification of three independent western blot results for N-cadherin upregulation. ***Indicates p < 0.001.

Fig 5: Kaplan–Meier overall survival curves for FGFR1 and FGFR2 protein expression and FGFR1–4 protein co-expression in oral cavity and oropharyngeal squamous cell carcinoma. a High FGFR1 (p = 0.018) protein expression and b high FGFR1–4 (p = 0.030) co-expression were related to poor overall survival in oral cavity squamous cell carcinoma in univariate analysis, but lost significance in multivariate analysis (FGFR1: HR 1.46; 95 % CI 0.91–2.34; p = 0.690, high expression: 151/305 died, low expression: 64/172 died, FGFR1–4: HR 2.44; 95 % CI 1.29–5.50; p = 0.060, high expression: 25/37 died, low expression: 165/399 died). c–f High FGFR2 (P = 0.084) protein expression was not related to overall survival in oral cavity squamous cell carcinoma (high expression: 118/238 died, low expression: 94/239 died). High FGFR1 (p = 0.630) expression, high FGFR1–4 (p = 1.000) co-expression and high FGFR2 (p = 1.000) expression were not related to overall survival in oropharyngeal squamous cell carcinoma (FGFR1: high expression: 148/287 died, low expression: 25/76 died, FGFR1–4: high expression: 45/88 died, low expression: 107/224 died and FGFR2: high expression: 107/225 died, low expression: 61/127 died)